Moleküler Biyoloji ve Genetik Bölümü / Department of Molecular Biology and Genetics
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Publication BABA Pre-Treatment Before Drought Stress Revealed Tolerance Related Proteomic Alterations in Rice(Wiley, 2022) YALÇIN, HM; MAYTALMAN, S.; İHVAN, YF; GÜMÜŞ, TAMER; MERİÇ, SİNAN; AYAN, ALP; ATAK, ÇİMENPublication Biotic Stress-Tolerant Plants Through Small Rna Technology(Elsevier, 2020) ÇELİK, ÖZGE; MERİÇ, SİNAN; AYAN, ALP; ATAK, ÇİMENWith an increasing population around the world, the rapid loss of agricultural fields shows us the urgent importance of finding solutions to develop agricultural productivity. Besides industrialization, several effectors such as abiotic and biotic factors cause losses in crop productivity. Biotic factors threaten production and transportation of products worldwide. Bacteria, fungi, viruses, and oomycetes cause losses both pre- and postharvest. It is crucial to improve biotic stress-tolerant plants to overcome reduction in plant productivity. For many years, researchers focused on understanding plant defense mechanisms. Anatomical, physiological, and molecular adaptive mechanisms were investigated for several plant species. Besides the innate immunity mechanisms, including cross-talk, among the phytohormones to manage appropriate defense mechanisms against pathogens, new generation strategies in crop improvements are widely used in plant biotechnology. Although conventional breeding has importance in breeding new varieties, new technologies increase the possibility of success. Recently, new combinations of technologies have been proven effective to develop new cultivars. Small RNA technology is one of the developing crop improvement technologies relying on regulating specific genes together with their sequence identity. In this chapter, we focus on the small RNA technologies used in improvement of biotic stress-tolerant plants.Publication Epibrassinolide-Induced Autophagy Occurs in an Atg5-Independent Manner Due to Endoplasmic Stress Induction in MEF Cells(Springer, 2020) Adacan, Kaan; YERLİKAYA, PINAR OBAKAN; Çoker-Gürkan, Ajda; Kaya, Resul İsmail; Palavan-Ünsal, Narcin; ARISAN, ELİF DAMLAEpibrassinolide (EBR), a polyhydroxysteroid belongs to plant growth regulator family, brassinosteroids and has been shown to have a similar chemical structure to mammalian steroid hormones. Our findings indicated that EBR could trigger apoptosis in cancer cells via induction of endoplasmic reticulum (ER) stress, caused by protein folding disturbance in the ER. Normal cells exhibited a remarkable resistance to EBR treatment and avoid from apoptotic cell death. The unfolded protein response clears un/misfolded proteins and restore ER functions. When stress is chronic, cells tend to die due to improper cellular functions. To understand the effect of EBR in non-malign cells, mouse embryonic fibroblast (MEF) cells were investigated in detail for ER stress biomarkers, autophagy, and polyamine metabolism in this study. Evolutionary conserved autophagy mechanism is a crucial cellular process to clean damaged organelles and protein aggregates through lysosome under the control of autophagy-related genes (ATGs). Cells tend to activate autophagy to promote cell survival under stress conditions. Polyamines are polycationic molecules playing a role in the homeostasis of important cellular events such as cell survival, growth, and, proliferation. The administration of PAs has been markedly extended the lifespan of various organisms via inducing autophagy and inhibiting oxidative stress. Our data indicated that ER stress is induced following EBR treatment in MEF cells as well as MEF Atg5(-/-) cells. In addition, autophagy is activated following EBR treatment by targeting PI3K/Akt/mTOR in wildtype (wt) cells. However, EBR-induced autophagy targets ULK1 in MEF cells lacking Atg5 expression. Besides, EBR treatment depleted the PA pool in MEF cells through the alterations of metabolic enzymes. The administration of Spd with EBR further increased autophagic vacuole formation. In conclusion, EBR is an anticancer drug candidate with selective cytotoxicity for cancer cells, in addition the induction of autophagy and PA metabolism are critical for responses of normal cells against EBR.Publication Examination of Fatty Acid Metabolism and Induction of Epithelial-Mesenchymal Transition Pathway via Modulation of miR-33a Levels in Caki-1 and Caki-2 Renal Cell(Wiley, 2022) İNCE, İ.; KALABALIKOĞLU, E.; ŞAHİN, BURCU AYHAN; KILBAŞ, PELİN ÖZFİLİZ; RENCÜZOĞULLARI, ÖZGEPublication Examining the Relationship of Diabetes-Related Cytokine Levels and EMT in STAT5-overexpressed Panc-1 and MiaPaCa-2 Pancreatic Cancer Spheroid Models in Response to Celastrol Treatment(WİLEY, 2022) RENCÜZOĞULLARI, ÖZGE; SARIKAYA, E.N.; KAHYA, B.Publication Heavy Metal Stress-Responsive Phyto-miRNAs(Springer Science and Business Media B.V., 2020) ÇELİK, ÖZGE; AYAN, ALP; MERİÇ, SİNAN; ATAK, ÇİMENHeavy metal stress is a leading abiotic stress factor in the twenty-first century as a reflection of industrial developments and extensive urbanization. Plants adopt several adaptation mechanisms to cope with deleterious effects of heavy metal stress. Biosynthesis of amino acids/organic acids, phytochelatins (PCs), metallothioneins (MTs), heat-shock proteins (HSPs), metal chelators, chaperons, ABC-type transporters, and CDF family metal transporters are among the heavy metal binding or transporting mechanisms in plants. This chapter emphasizes phyto-miRNAs related to these tolerance mechanism pathways. Moreover, transcription factors which are targeted by heavy metal-related phyto-miRNAs are also summarized under the effect of various heavy metals due to their intertwined regulatory mechanisms.Publication Investigation of the Effect of STAT3 Inhibition on Apoptotic Process Associated with JAK/STAT Signaling Pathway in A-498 and ACHN Renal Carcinoma Cells(Wiley, 2022) YILDIZHAN, K. Y.; AYDIN, Y. E.; KILBAŞ, PELİN ÖZFİLİZ; ŞAHİN, BURCU AYHAN; RENCÜZOĞULLARI, ÖZGEPublication Proinflammatory Cytokine Profile is Critical in Autocrine GH-Triggered Curcumin Resistance Engulf by Atiprimod Cotreatment in MCF-7 and MDA-MB-231 Breast Cancer Cells(Springer, 2020) Çoker-Gürkan, Ajda; Özakaltun, Buse; Akdeniz, Berre-Serra; Ergen, Berfin; YERLİKAYA, PINAR OBAKAN; Akkoç, Tunç; ARISAN, ELİF DAMLAActive growth hormone (GH) signaling triggers cellular growth and invasion-metastasis in colon, breast, and prostate cancer. Curcumin, an inhibitor of NF-kappa B pathway, is assumed to be a promising anti-carcinogenic agent. Atiprimod is also an anti-inflammatory, anti-carcinogenic agent that induces apoptotic cell death in hepatocellular carcinoma, multiple myeloma, and pituitary adenoma. We aimed to demonstrate the potential additional effect of atiprimod on curcumin-induced apoptotic cell death via cytokine expression profiles in MCF-7 and MDA-MB-231 cells with active GH signaling. The effect of curcumin and/or atiprimod on IL-2, IL-4, and IL-17A levels were measured by ELISA assay. MTT cell viability, trypan blue exclusion, and colony formation assays were performed to determine the effect of combined drug exposure on cell viability, growth, and colony formation, respectively. Alteration of the NF-kappa B signaling pathway protein expression profile was determined following curcumin and/or atiprimod exposure by RT-PCR and immunoblotting. Finally, the effect of curcumin with/without atiprimod treatment on Reactive Oxygen Species (ROS) generation and apoptotic cell death was examined by DCFH-DA and Annexin V/PI FACS flow analysis, respectively. Autocrine GH-mediated IL-6, IL-8, IL-10 expressions were downregulated by curcumin treatment. Atiprimod co-treatment increased the inhibitory effect of curcumin on cell viability, proliferation and also increased the curcumin-triggered ROS generation in each GH(+) breast cancer cells. Combined drug exposure increased apoptotic cell death through acting on IL-2, IL-4, and IL-17A secretion. Forced GH-triggered curcumin resistance might be overwhelmed by atiprimod and curcumin co-treatment via modulating NF-kappa B-mediated inflammatory cytokine expression in MCF-7 and MDA-MB-231 cells.Publication The Role of the PI3K/AKT/mTOR Signaling Axis in the Decision of the Celastrol-Induced Cell Death Mechanism Related to the Lipid Regulatory Pathway in Prostate Cancer Cells(Elsevier, 2020) RENCÜZOĞULLARI, ÖZGE; Çoban, Mervenur; Sevgin, Bortecine; Çoker-Gürkan, Ajda; YERLİKAYA, PINAR OBAKAN; Palavan-Ünsal, Narcin; ARISAN, ELİF DAMLAProstate cancer is one of the leading cancer types among the male population worldwide, with high incidence and mortality rates. Celastrol is a promising bioactive component extracted from Tripterygium wilfordi. Celastrol is a multimodal agent with therapeutic advantages, with activities that affect cell proliferation, inflammation (through affecting proteotoxic stress) and cell death mechanisms such as autophagy, apoptosis and paraptosis. Celastrol alters the PI3K/AKT signaling axis to suppress the cell viability of cancer cells. Although a number of celastrol targets have been identified in cancer cells, the genomic differences in malignant cells prevent the efficacy of celastrol. Therefore, new studies are required to highlight its potential therapeutic effects in cancer cells. In this study, we investigated the therapeutic potential of celastrol in LNCaP, DU145 and PC3 prostate cancer cells. According to our results, celastrol decreased cell viability in a dose-dependent manner in the cells. LNCaP prostate cancer cells were more sensitive to celastrol treatment compared to DU145 and PC3 cells. We found that celastrol modulated PI3K/AKT/mTOR signaling to alter lipid regulatory pathways by affecting LAMP -1 and lipin-1 in PC3 cells. Although celastrol downregulated FASN in all cell lines, active mTOR signaling led to altered responses in prostate cancer cells by affecting the cellular fate decision pathways.Publication Targeting Fatty Acid Metabolism-Associated EMT Signaling by Palbociclib in Combination with Celastrol in Pancreatic Cancer Cells(2022) DELİOĞLU, S. S.; GİRİTLİOĞLU, Z.; RENCÜZOĞULLARI, ÖZGE